Abstract
Orofacial pain represents a significant clinical burden, with current pharmacological treatments limited by adverse effects and insufficient efficacy. Dental pulp mesenchymal stromal cell–derived extracellular vesicles (DPMSC-EVs) offer a promising cell‑free therapeutic alternative due to their anti‑inflammatory and neuroprotective properties. This thesis evaluated the potential of DPMSC-EVs to modulate neuroinflammatory pain mechanisms using an in vitro human neuronal pain model. DPMSC-EVs were isolated, characterised, and shown to be biocompatible. Functional assays indicated that EV treatment attenuated inflammatory mediator release and reduced neuronal hypersensitivity associated with TRP channel activation. Transcriptomic and bioinformatic analyses highlighted NF‑κB signalling as a key pathway influenced by EVs, with specific miRNAs implicated as potential mediators. Together, these findings support DPMSC-EVs as a biocompatible, cell‑free strategy for targeting neuroinflammatory components of orofacial pain.Thesis is embargoed until 31 December 2031.
| Date of Award | Dec 2026 |
|---|---|
| Original language | English |
| Awarding Institution |
|
| Sponsors | Applied Science Private University Jordan |
| Supervisor | Ikhlas El Karim (Supervisor), Anna Krasnodembskaya (Supervisor) & Fionnuala Lundy (Supervisor) |
Keywords
- Stem Cells
- EVs
- DPC-EV
- MSC-EV
- Orofacial Pain
- TRP Channels
- TRPV1
- TRPV2
- TRPM8
- RNA sequencing
- SH-SY5Y cells
- neuroinflammation
- stem cell therapy
- ibuprofen
- pain
- pain signalling
- calcium signalling
- Fura2
- SEC
- size exclusion chromatography
- dental pain
- oral pain
- oral health
- TRPC5
- TRPV4
- hypersensitivity
- pulpal pain
- periodontal pain
- DPMSC-EVs
- DPMSC
- Extracellular vesicles
- Conditioned media
- hyperactivity
- Pain signal
- dental pulp cells
- dental pulp mesenchymal stromal cells
- extracellular vesicles derived from DPMSC
- DPMSC-EV
- mRNA
- ELISA
- RT-PCR
- ICC
- NTA
- TEM
- neuronal sensitisation
- neuronal pain
- TNFa
- NFkB
- hDPCs
- IL8
- CCL2
- p65
- qEV
- SH-SY5Y
- TRAF1
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